Association between Helicobacter pylori infection and pancreatic cancer. M Raderer, F Wrba, G Kornek, T Maca, DY Koller, G Weinlaender, M Hejna, W Scheithauer. Oncology 1998 Jan-Feb;55(1):16-19. 65% of 92 patients with pancreatic adenocarcinoma, and 69% of 30 with gastric cancer, were seropositive for HP, versus 45% of other controls (35 with colorectal cancer and 27 healthy volunteers). OR= 2.1 (1.1-4.1), p=0.035.

Detection of Helicobacter DNA in bile from bile duct diseases. IH Roe, JT Kim, HS Lee, JH Lee. J Korean Med Sci 1999;14:182-186. HP DNA was detected in 7/15 bile duct cancers, 2/6 pancreatic head cancers, and 3/11 cases of intrahepatic duct stones.

Helicobacter pylori seropositivity as a risk factor for pancreatic cancer. RZ Stolzenberg-Solomon, MJ Blaser, PJ Limburg, G Perez-Perez, PR Taylor, J Virtamo, D Albanes. J Natl Cancer Inst 2001 Jun 20;93(12):937-941. 82% of 121 cases versus 73% of 226 controls were positive for HP, OR 2.01 (1.09-3.70) with CagA+ strains.

Helicobacter species ribosomal DNA in the pancreas, stomach and duodenum of pancreatic cancer patients. HO Nilsson, U Stenram, I Ihse, T Wadstrom. World J Gastroenterol 2006 May 21;12(19):3038-3043. "Patients with exocrine pancreatic cancer (n = 40), neuroendocrine cancer (n = 14), multiple endocrine neoplasia type 1 (n = 8), and chronic pancreatitis (n = 5) were studied. Other benign pancreatic diseases (n = 10) and specimens of normal pancreas (n = 7) were included as controls.... Helicobacter DNA was detected in pancreas (tumor and/or surrounding tissue) of 75% of patients with exocrine cancer, 57% of patients with neuroendocrine cancer, 38% of patients with multiple endocrine neoplasia, and 60% of patients with chronic pancreatitis. All samples from other benign pancreatic diseases and normal pancreas were negative. Thirty-three percent of the patients were helicobacter-positive in gastroduodenal specimens. Surprisingly, H. bilis was identified in 60% of the positive gastroduodenal samples. All gallbladder and ductus choledochus specimens were negative for helicobacter." "DNA of different Helicobacter species in the pancreas compared with gastroduodenal tissue was identified in patients who were Helicobacter-positive both in the stomach and pancreas. Moreover, many pancreas-positive PC patients were negative in stomach samples and vice versa, not supporting migration of helicobacter microorganisms colonizing the stomach to the pancreas in the studied PC patients."

The risk of pancreatic cancer in patients with gastric or duodenal ulcer disease. J Luo, C Nordenvall, O Nyrén, HO Adami, J Permert, W Ye. Int J Cancer 2007 Jan 15;120(2):368-372. "During years 3-38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10-40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10-110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4-3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy."

Helicobacter pylori infection and development of pancreatic cancer. C de Martel, AE Llosa, GD Friedman, JH Vogelman, N Orentreich, RZ Stolzenberg-Solomon, J Parsonnet. Cancer Epidemiol Biomarkers Prev 2008 May;17(5):1188-1194. 104 randomly selected subjects among 507 who developed pancreatic cancer, and 262 pancreatic cancer–free subjects from a pool of 730 controls in the Kaiser Permanente Medical Care Program, by serology. "Neither H. pylori [odds ratio (OR), 0.85; 95% confidence interval (95% CI), 0.49-1.48] nor its CagA protein (OR, 0.96; 95% CI, 0.48-1.92) was associated with subsequent development of pancreatic cancer." Among a number of peculiar findings, the most peculiar was a supposedly higher risk from a college education, than from smoking!

A prospective study of Helicobacter pylori in relation to the risk for pancreatic cancer. B Lindkvist, D Johansen, A Borgström, J Manjer. BMC Cancer 2008 Nov 5;8:321. 87 cases and 263 controls, by serology from stored samples. "H. pylori seropositivity was not associated with pancreatic cancer in the total cohort (adjusted OR 1.25 (0.75–2.09)). However, a statistically significant association was found in never smokers (OR 3.81 (1.06–13.63) adjusted for alcohol consumption) and a borderline statistically significant association was found in subjects with low alcohol consumption (OR 2.13 (0.97–4.69) adjusted for smoking)." "There was a slightly higher proportion of current smokers among H. pylori positive subjects." "In the small subgroup of subjects who reported a low risk alcohol consumption and were never smokers (8 cases and 55 controls), the crude OR for pancreatic cancer related to a positive H. pylori serology was 13.20 (2.31–75.31) (not shown in table)."

ABO Blood Group, Helicobacter pylori Seropositivity, and Risk of Pancreatic Cancer: A Case-Control Study. HA Risch, H Yu, L Lu, MS Kidd. J Natl Cancer Inst 2010 Apr 7;102(7):502-505. 373 cases and 690 controls. "Increased risk of pancreatic cancer was associated with non-O blood group (adjusted odds ratio [OR] = 1.37, 95% confidence interval [CI] = 1.02 to 1.83, P = .034) and CagA-negative H pylori seropositivity (OR = 1.68, 95% CI = 1.07 to 2.66, P = .025), but no association was observed for CagA seropositivity (OR = 0.77, 95% CI = 0.52 to 1.16). An association between pancreatic cancer risk and CagA-negative H pylori seropositivity was found among individuals with non-O blood type but not among those with O blood type (OR = 2.78, 95% CI = 1.49 to 5.20, P = .0014; OR = 1.28, 95% CI = 0.62 to 2.64, P = .51, respectively). This study demonstrates an association between pancreatic cancer and H pylori colonization, particularly for individuals with non-O blood types."

Helicobacter pylori in autoimmune pancreatitis and pancreatic carcinoma. R Jesnowski, B Isaksson, C Möhrcke, C Bertsch, M Bulajic, W Schneider-Brachert, G Klöppel, AB Lowenfels, P Maisonneuve, JM Löhr. Pancreatology 2010;10(4):462-466. 35 pancreatic juice samples and 30 pancreatic tissues. "In the pancreas of 11 patients with autoimmune pancreatitis, no H. pylori DNA could be detected. Further, in none of the other tissue samples of chronic pancreatitis or PDAC [pancreatic ductal adenocarcinoma] could we detect any Helicobacter sequences. Out of the pancreatic juice samples, none demonstrated either of the 2 Helicobacter gene sequences investigated."

Association between Helicobacter pylori infection and pancreatic cancer. A cumulative meta-analysis. G Trikudanathan, A Philip, CA Dasanu, WL Baker. JOP 2011 Jan 5;12(1):26-31. Six studies involving 2,335 patients. "A significant association between H. pylori seropositivity and development of pancreatic cancer (AOR 1.38, 95% CI: 1.08-1.75; P=0.009) was seen. No significant association was seen on pooled analysis of the three studies assessing the relationship between cytotoxin-associated gene A (CagA) positivity and pancreatic cancer. A cumulative meta-analysis suggested a reducing, albeit statistically significant association as the evidence was accumulated."

Helicobacter is implicated in biliary tract disease

Bacteria closely resembling Helicobacter pylori detected immunohistologically and genetically in resected gallbladder mucosa. M Kawaguchi, T Saito, H Ohno, S Midorikawa, T Sanji, Y Handa, S Morita, H Yoshida, M Tsurui, R Misaka, T Hirota, M Saito, K Minami. J Gastroenterol 1996 Apr;31(2):294-298. "A microorganism with close immunohistological and genetic resemblance to Helicobacter pylori was found in the resected gallbladder mucosa of a 41-year-old woman." It was detected incidentally on pathological examination.

Hepatic Helicobacter species identified in bile and gallbladder tissue from Chileans with chronic cholecystitis. JG Fox, FE Dewhirst, Z Shen, Y Feng, NS Taylor, BJ Paster, RL Ericson, CN Lau, P Correa, JC Araya, I Roa. Gastroenterology 1998 Apr;114(4):755-763. 9 of 23 gallbladder tissues were positive for Helicobacter by PCR. By phylogenetic analysis, five represented strains of H. bilis, two of "Flexispira rappini" (ATCC 49317), and one of H. pullorum.

Are infectious agents involved in primary biliary cirrhosis? A PCR approach. A Tanaka, TP Prindiville, R Gish, JV Solnick, RL Coppel, EB Keeffe, A Ansari, ME Gershwin. J Hepatol 1999 Oct;31(4):664-671. 29 patients with primary biliary cirrhosis, versus "patients with primary sclerosing cholangitis, chronic hepatitis, alcoholic liver disease and otherwise normal donors." "Neither Archaeabacteria nor Mycobacteria products were detected in liver specimens of patients with primary biliary cirrhosis, and Helicobacter pylori DNA was detected in only one primary biliary cirrhosis patient."

Identification of Helicobacter pylori and other Helicobacter species by PCR, hybridization, and partial DNA sequencing in human liver samples from patients with primary sclerosing cholangitis or primary biliary cirrhosis. HO Nilsson, J Taneera, M Castedal, E Glatz, R Olsson, T Wadstrom. J Clin Microbiol 2000 Mar;38(3):1072-1076. 9/12 patients with primary sclerosing cholangitis and 11/12 with primary biliary cirrhosis were positive by PCR with Helicobacter genus-specific primers, versus 1/13 with noncholestatic liver cirrhosis and 0/10 normal livers (P = <0.00001).

Lack of association between Helicobacter sp colonization and gallstone disease. N Méndez-Sánchez, R Pichardo, J González, H Sánchez, M Moreno, F Barquera, HO Estevez, M Uribe. J Clin Gastroenterol 2001 Feb;32(2):138-141. "Only 1 of the 95 specimens was positive for Helicobacter by immunohistochemistry analysis; 1 of 32 cases, by PCR."

Identification of Helicobacter pylori DNA in human cholesterol gallstones. HJ Monstein, Y Jonsson, J Zdolsek, J Svanvik. Scand J Gastroenterol 2002 Jan;37(1):112-119. "Cholesterol gallstones from 20 patients were subjected to polymerase chain reaction, bacterial profiling by temporal temperature gradient gel electrophoresis, automated DNA sequencing, and Southern blot analysis using a Helicobacter sp. specific primer. A nested ureI-PCR assay was used to discriminate between gastric and non-gastric H. pylori. RESULTS: TTGE, partial 16S rDNA sequencing, and hybridization analysis revealed the presence of DNA presumably representing a mixed bacterial flora in cholesterol gallstones, including H. pylori in the gallstone centres in 11 out of 20 patients. In three cases, the urel-PCR assay revealed non-gastric H. pylori."

Association between Helicobacter bilis in bile and biliary tract malignancies: H. bilis in bile from Japanese and Thai patients with benign and malignant diseases in the biliary tract. N Matsukura, S Yokomuro, S Yamada, T Tajiri, T Sundo, T Hadama, S Kamiya, Z Naito, JG Fox. Jpn J Cancer Res 2002 Jul;93(7):842-847. "Thirteen out of 15 (87%) Japanese and 11 out of 14 (79%) Thai patients with bile duct or gallbladder cancer tested positive for the presence of H. bilis in their bile. Eight out of 16 (50%) Japanese and 10 out of 26 (38%) Thai patients with gallstone and / or cholecystitis tested positive for H. bilis. Only 4 out of 14 (29%) subjects without biliary disease tested positive for H. bilis among the Japanese. Bile duct and gallbladder cancer showed significantly higher positive rates for H. bilis than did the non-biliary diseases among the Japanese (P < 0.01) and the odds ratios for bile duct or gallbladder cancer with H. bilis in comparison with gallstone and / or cholecystitis were 6.50 (95%CI 1.09 - 38.63) in the Japanese and 5.86 (1.31 - 26.33) in the Thai patients."

Helicobacter pylori and the risk of benign and malignant biliary tract disease. M Bulajic, P Maisonneuve, W Schneider-Brachert, P Muller, U Reischl, B Stimec, N Lehn, AB Lowenfels, M Lohr. Cancer 2002 Nov 1;95(9):1946-1953. 89 patients: 63 with biliary calculi, 15 with carcinoma of the biliary tract, and 11 with neither gallstones nor carcinoma. "Patients with gallstones were 3.5 times as likely to have H. pylori in the bile compared with patients in a control group (95% confidence interval [95%CI], 0.8-15.8; P = 0.100), and H. pylori was 9.9 times more frequent in patients with biliary tract carcinoma compared with patients in the control group (95%CI, 1.4-70.5; P = 0.022)."

Helicobacter DNA in bile: correlation with hepato-biliary diseases. CA Fallone, S Tran, M Semret, F Discepola, M Behr, AN Barkun. Aliment Pharmacol Ther 2003 Feb;17(3):453-458. Bile collected from 75 patients with biliary stones, 15 with pancreatico-biliary malignancies and four with primary sclerosing cholangitis. "Helicobacter was detected in all positive controls. Only three samples had polymerase chain reaction inhibitors. All remaining bile samples (122 patients with hepato-biliary diseases) were negative for Helicobacter DNA."

Common presence of Helicobacter DNA in the gallbladder of patients with gallstone diseases and controls. W Chen, D Li, RJ Cannan, RS Stubbs. Dig Liver Dis 2003 Apr;35(4):237-243. By PCR in gallbladder samples and by enzyme linked immunosorbent assay in serum and bile, "Helicobacter DNA was detected in 61 (50.0%) gallbladder samples: 29 of 60 (48.3%) patients with symptomatic gallstone, six of 10 (60.0%) patients with asymptomatic gallstones, 11 of 15 (73.3%) patients with other biliary diseases, and 15 of 37 (40.5%) control patients, respectively. Among them, 39 samples were positive for Helicobacter pylori but none were positive for Helicobacter bilis. Sequence analysis of Helicobacter genus-positive samples showed that 56 samples were Helicobacter pylori and five were Helicobacter species 'Liver 3' strain. Overall, there was no significant difference in the detection rate of Helicobacter DNA or the levels of serum and bile Helicobacter pylori-specific immunoglobulin G in the various biliary disease groups compared with control patients."

Association of the presence of Helicobacter in gallbladder tissue with cholelithiasis and cholecystitis. CP Silva, JC Pereira-Lima, AG Oliveira, JB Guerra, DL Marques, L Sarmanho, MM Cabral, DM Queiroz. J Clin Microbiol 2003 Dec;41(12):5615-5618. Nested PCR of 16S rRNA genes in gallbladder tissue and bile from 46 Brazilian subjects with and 18 without cholelithiasis. "When the logistic regression model was applied in the multivariate analysis, cholelithiasis remained independently associated with increasing age (P = 0.002; odds ratio [OR] = 1.07; 95% confidence interval [CI] = 1.03 to 1.12), female gender (P = 0.02; OR = 5.68; 95% CI = 1.38 to 23.49), and the presence of H. pylori DNA in the gallbladder tissue (P = 0.009; OR = 14.72; 95% CI = 1.97 to 108.90)."

Helicobacter bilis infection in biliary tract cancer. H Murata, S Tsuji, M Tsujii, HY Fu, H Tanimura, M Tsujimoto, N Matsuura, S Kawano, M Hori. Aliment Pharmacol Ther 2004 Jul;20 Suppl 1:90-94. Archival gallbladder specimens from 34 patients (14 males and 20 females), "consisting of 11 cases of gallbladder cancer, three of bile duct cancer, 16 of cholecystolithiasis and four of pancreatic cancer. DNA was extracted and nested PCR using primers specific for 16S rRNA of H. bilis was performed. RESULTS: Amplification was observed in 3 of 11 gallbladder cancer cases (27.2%) and one of three cases with biliary duct cancer (33.3%). In total, four of 14 cases with biliary tract cancer were positive for H. bilis (28.6%). In addition, the presence of H. bilis was shown in two of 16 cases (12.5%) with cholecystolithiasis. Notably, although the number of cases examined was small, none of the four cases with pancreatic cancer showed the presence of H. bilis infection in the gallbladder without apparent abnormalities."

Relation between gallbladder neoplasm and Helicobacter hepaticus infection. SB Pradhan, S Dali. Kathmandu Univ Med J (KUMJ) 2004 Oct-Dec;2(4):331-335. Of 100 cases that were willing to provide gallbladder for study; "82% cases were found to have Helicobacter hepaticus infection. Only one out of 7 malignant cases (14.29%) was found to be negative for Helicobacter Hepaticus infection."

Identification of Helicobacter pylori DNA in Iranian patients with gallstones. Sh Farshad, A Alborzi, SA Malek Hosseini, B Oboodi, M Rasouli, A Japoni, J Nasiri. Epidemiol Infect 2004 Dec;132(6):1185-1189. Gallstone and bile samples from 33 patients and 40 normal autopsied gallbladders. H. pylori DNA was detected by PCR in 18.1% of stone and 12.1% of bile samples. The PCR was negative in the control group.

Helicobacter pylori and other Helicobacter species in gallbladder and liver of patients with chronic cholecystitis detected by immunological and molecular methods. E Apostolov, WA Al-Soud, I Nilsson, I Kornilovska, V Usenko, V Lyzogubov, Y Gaydar, T Wadström, A Ljungh. Scand J Gastroenterol 2005 Jan;40(1):96-102. In gallbladder and liver biopsy specimens from 22 adult Ukrainian patients with chronic cholecystitis, "Helicobacter DNA was found in 16/22 (73%) of the gallbladder samples and in 11/22 (50%) of the liver samples. IHC showed the presence of the H. pylori specific cytotoxins CagA and VacA inside the gallbladder epithelial cells without co-localization of H. pylori at the epithelial lining."

Helicobacter pylori in the etiology of cholesterol gallstones. B Abayli, S Colakoglu, M Serin, S Erdogan, YF Isiksal, I Tuncer, F Koksal, H Demiryurek. J Clin Gastroenterol 2005 Feb;39(2):134-137. "Different bacterium were isolated from 22 gallbladder samples (12 Escherichia coli, 8 Pseudomonas, and 2 clostridium) and H. pylori was isolated in 6 gallbladder samples. Helicobacter spp was found in 7 gallstones by PCR amplification. Helicobacter-like organisms were demonstrated in 18 samples by three different histopathologic methods. Helicobacter-like organisms were also found in five samples by the same histopathologic methods (Warthin-Starry, hematoxylin-eosin, and gram staining). Only four samples were found positive for Helicobacter spp/H. pylori by all methods."

The role of Helicobacter spp. in the pathogenesis of primary biliary cirrhosis and primary sclerosing cholangitis. SY Boomkens, S de Rave, RG Pot, HF Egberink, LC Penning, J Rothuizen, PE Zondervan, JG Kusters. FEMS Immunol Med Microbiol 2005 May 1;44(2):221-225. 18 patients with PBC, 13 with PSC, versus 29 patient controls (9 with hepatitis B, 14 with alcoholic cirrhosis, 6 with non-cirrhotic metabolic liver disease. "There was no significant difference between the incidence of Helicobacter spp.-specific DNA in PBC/PSC (9/31; 29%) and the control group (10/29; 34%)." [Patient controls may have had high rates of infection -cast].

Gallbladder cancer worldwide: geographical distribution and risk factors. G Randi, S Franceschi, C La Vecchia. Int J Cancer 2006 Apr 1;118(7):1591-602. Review. "History of gallstones was the strongest risk factor for gallbladder cancer, with a pooled relative risk (RR) of 4.9 [95% confidence interval (CI): 3.3-7.4]. Consistent associations were also present with obesity, multiparity and chronic infections like Salmonella typhi and S. paratyphi [pooled RR 4.8 (95% CI: 1.4-17.3)] and Helicobacter bilis and H. pylori [pooled RR 4.3 (95% CI: 2.1-8.8)]. Differences in incidence ratios point to variations in gallbladder cancer aetiology in different populations."

Helicobacter pylori and other Helicobacter species DNA in human bile samples from patients with various hepato-biliary diseases. SK Tiwari, AA Khan, M Ibrahim, MA Habeeb, CM Habibullah. World J Gastroenterol 2006 Apr 14;12(14):2181-2186. Sixty bile samples were obtained from patients diagnosed with various hepato-biliary diseases and control subjects with various gastric disorders. "No Helicobacters were grown in culture from the bile samples. Helicobacter DNA was detected in bile of 96.7% and 6.6% of groups I and II respectively."

H pylori exist in the gallbladder mucosa of patients with chronic cholecystitis. DF Chen, L Hu, P Yi, WW Liu, DC Fang, H Cao. World J Gastroenterol 2007 Mar 14;13(10):1608-1611. Paraffin specimens of 524 cases of cholecystitis screened by Warthy-Starry (W-S) silver stain and immunohistochemistry stain with anti-H pylori antibodies; and fresh tissue specimens from 81 cases of cholecystitis analyzed by PCR. "H pylori-like bacteria were found in 13.55% of the gallbladders of the cholecystitis patients using W-S stain. Meanwhile, bacteria positive for H pylori antibodies were also found in 7.1% of the gallbladders of patients with cholecystitis by immunohistochemistry. Of 81 gallbladders, 11 were positive for both HPUA and HPUB, 4 were positive for HPUA only and 7 were positive for HPUB only."

Low prevalence of Helicobacteraceae in gall-stone disease and gall-bladder carcinoma in the German population. UR Bohr, d Kuester, f Meyer, T Wex, M Stillert, A Csepregi, H Lippert, A Roessner, P Malfertheiner. Clin Microbiol Infect 2007 May;13(5):525-531. 57 cases of gall-stone disease, 20 cases of GBC, and 22 control patients. "Of the 99 cases investigated, only one patient with GSD was PCR-positive for Helicobacteraceae."

Helicobacter pylori in areas of gastric metaplasia in the gallbladder and isolation of H. pylori DNA from gallstones. V Misra, SP Misra, M Dwivedi, Y Shouche, M Dharne, PA Singh. Pathology 2007 Aug;39(4):419-24. 111 gallbladders with evidence of gastric metaplasia; "Helicobacter pylori was present in 50 of 111 (45%) sections with gastric metaplasia. Areas adjacent to gastric metaplasia in gallbladder showed acute inflammation (6%) and lymphoid follicle formation in 58% of cases with H. pylori that were significantly higher than those seen in sections without H. pylori. In molecular study, 8 of 11 gallstones showed 16S rDNA."

Helicobacter species are associated with possible increase in risk of biliary lithiasis and benign biliary diseases. M Pandey. World J Surg Oncol 2007 Aug 20;5:94. Review. "A total of 12 articles were identified. One study used IgG for diagnosis while others used the PCR for Ure A gene, 16 S RNA or Cag A genes. A couple of studies used culture or histopathology besides the PCR. The cumulative results show a higher association of Helicobacter with chronic liver diseases (30.48%), and stone diseases (42.96%)(OR 1.77 95% CI 1.2-2.58; Z = 2.94, p = 0.003), the effect of each could not be identified as it was difficult to isolate the effect of helicobacter due to mixing of cases in each study."

Helicobacter pylori may play a contributory role in the pathogenesis of primary sclerosing cholangitis. AM Krasinskas, Y Yao, P Randhawa, MP Dore, AR Sepulveda. Dig Dis Sci 2007 Sep;52(9):2265-2270. 25 patients with end-stage PSC and 31 controls. "Seven of the 25 (28%) patients with PSC and 3 of the 31 (9.7%) controls were positive for Helicobacter (P=.087). H pylori DNA was detected in microdissected hilar biliary epithelium in more PSC patients than controls...."

Helicobacter species in cancers of the gallbladder and extrahepatic biliary tract. C de Martel, M Plummer, J Parsonnet, LJ van Doorn, S Franceschi. Br J Cancer 2009 Jan 13;100(1):194-199. Review. "Nine studies of BT cancers were identified, all with 30 or fewer BT cancers; eight included cancer-free control subjects and used polymerase chain reaction (PCR) as a means of Helicobacter species detection. In four of these studies, Helicobacter species were detected in patients with BT cancer significantly more frequently than in controls, at least when controls without BT diseases were used. In two studies, no Helicobacter species were detected in either cases or controls. Helicobacter species were also often detected in benign BT diseases such as gallstone disease or chronic cholecystitis."

Helicobacter species are associated with possible increase in risk of hepatobiliary tract cancers. M Pandey, M Shukla. Surg Oncol 2009 Mar;18(1):51-56. Review. "The cumulative sample size of cases was 205, of which 115 were positive (56%) for Helicobacter, while among 263 controls 53 (20%) were found to be positive for Helicobacter infection. The positivity rate in case control studies was higher than that observed in single group studies. The cumulative odds ratio for the study sample was 8.72 (95% CI 4.78-15.91) (Z=7.07; p<0.00001). CONCLUSIONS: There is enough evidence to suggest a possible role of Helicobacter species in hepatobiliary tract cancers. However, the results from different regions of the world differ. Studies also differ on method of Helicobacter detection, subsite of cancer with in the hepatobiliary tract and choice of controls thus introducing heterogeneity. Further case control studies with larger sample size are required to settle the question."

Helicobacter species DNA in liver and gastric tissues in children and adolescents with chronic liver disease. TH Casswall, A Németh, I Nilsson, T Wadström, HO Nilsson. Scand J Gastroenterol 2010;45(2):160-167. "The Helicobacter PCR was positive in 3/23 (13%) livers from patients with primary sclerosing cholangitis and UC, and in 1/2 livers from patients with autoimmune hepatitis (AIH) and UC. Sequenced PCR products matched the 16S rDNA of H. hepaticus, H. muridarum, H. canis, and H. pylori, respectively. H. ganmani and H. bilis were detected in gastric tissues from two AIH patients. H. hepaticus and H. pullorum were found in livers from two patients with acute liver failure and intrahepatic cholestasis."

Serological analysis of Helicobacter hepaticus infection in patients with biliary and pancreatic diseases. T Shimoyama, R Takahashi, D Abe, I Mizuki, T Endo, S Fukuda. J Gastroenterol Hepatol 2010 May;25 Suppl 1:S86-89. Serum from 55 patients with cholelithiasis, 18 with bile duct or gallbladder cancer and 19 with pancreatic cancer, and 34 controls. "Prevalence of antibody to H. hepaticus-specific antigen in patients with bile tract cancer was 38.8% and was significantly higher than in control subjects (13.1%, P < 0.05). Prevalence of antibody to H. hepaticus-specific antigen was 18.2% and 10.5% in patients with cholelithiasis and pancreatic cancer, respectively. Seropositivity for H. pylori was similar in all groups."

Other bacteria

Role of bile bacteria in gallbladder carcinoma. V Sharma, VS Chauhan, G Nath, A Kumar, VK Shukla. Hepatogastroenterology 2007 Sep;54(78):1622-1625. Bile culture in 65 gallbladder carcinoma patients, 125 cholelithiasis patients, and 200 controls. "Significantly higher number of patients with gallbladder carcinoma 40 (65%) had culture positive bile as compared to cholelithiasis 52 (42%) and control 24 (12%). Vi Antibodies suggestive of chronic typhoid carrier state were found to be significantly higher in the gallbladder carcinoma group 20 (31%) as compared to controls 22 (11%) (OR 3.596, p < 0.05) however, the difference was statistically insignificant in the cholelithiasis group 12 (11%) (OR 0.859, p > 0.05). There was a 6.84 times higher risk of developing gallbladder carcinoma in culture positive cholelithiasis patients and 5.14 times if both Vi antibody and cultures were positive." Levels of primary bile acids were lower and secondary bile acids were higher in the gallbladder carcinoma group.

cast 01-27-11